Jacobio Pharmaceuticals Group Co., Ltd. · HKEX:1167

Jacobio Pharmaceuticals — FY2023 Earnings Presentation

36 slides from Jacobio Pharmaceuticals's earnings presentation, April 2024

  1. Slide 1: Jacobio 2023 Annual Presentation

    Jacobio 2023 Annual Presentation April 2024 1167.HK

  2. Slide 2: Disclaimer

    Disclaimer This presentation includes forward-looking statements. All statements contained in this presentation other than statements of historical facts, including statements regarding future results of operations and financial position of Jacobio Pharmaceuticals (“Jacobio” “we,” “us” or “our”), ou

  3. Slide 3: Key Milestones and Catalyst Events

    Key Milestones and Catalyst Events 2022 Annual Results

  4. Slide 4: 2023 Annual Results

    2023 Annual Results Glecirsaib (JAB-21822, KRAS G12C inhibitor) Other clinical programs & JAB-3312 (SHP2 inhibitor) JAB-8263 (BET inhibitor)  Patient enrollment for pivotal trial finished in Sep 2023. ≥2L NSCLC  Pre-NDA submission of CMC portion finished in Sep  Efficacy: Clinical benefits observ

  5. Slide 5: 2023 Annual Results

    2023 Annual Results 2023 ESMO (Oral Presentation) 2023 JCA-AACR (Poster Presentation)  Glecirasib in combination with JAB-3312 in patients with  Glecirasib monotherapy and in combination with cetuximab KRAS G12C mutated solid tumors in patients with advanced colorectal cancer 144 patients enrolled

  6. Slide 6: 2024 Key Milestones and Catalyst Events (1/2)

    2024 Key Milestones and Catalyst Events (1/2) Events Expected Timing NDA submission Glecirasib (JAB-21822) monotherapy in ≥2L NSCLC Q2 2024 Pivotal trials Glecirasib (JAB-21822) in combination with JAB-3312 to treat 1L NSCLC: Phase III registrational trial initiation Q3 2024 Glecirasib (JAB-21822) m

  7. Slide 7: 2024 Key Milestones and Catalyst Events (2/2)

    2024 Key Milestones and Catalyst Events (2/2) Data publication Expected Timing Clinical data publication Long-term safety and efficacy data of glecirasib in combination with June 2024 ASCO JAB-3312 in solid tumors (oral presentation) Clinical data of JAB-8263 dose escalation/expansion June 2024 EHA

  8. Slide 8: Technology Platform

    Technology Platform  Leveraging our IADD platform for developing novel drugs toward “undruggable" targets and serving as payloads for iADC iADC STING agonist TAA antibody In-house iADC products with innovative payloads developed Jabobio’s Induced Allosteric Drug Discovery (IADD) utilizing IADD plat

  9. Slide 9: Pipeline Focusing on Oncogenic Pathways

    Pipeline Focusing on Oncogenic Pathways Pathway Asset Target Status Indication JAB-3312 SHP2 Phase III 1L NSCLC (combined with JAB-21822) JAB-21822 (Glecirasib) KRAS G12C NDA in Q2 2024 ≥2L NSCLC Pivotal Phase II ≥2L PDAC Phase III 1L NSCLC (combined with JAB-3312) RAS JAB-23E73 KRASmulti IND enabli

  10. Slide 10: Targeting “Undruggable” Targets

    Targeting “Undruggable” Targets 2022 Annual Results

  11. Slide 11: Global Competitive Landscape of KRAS G12C Inhibitors

    KRAS G12Ci SHP2i KRASmultii p53a BETi AURKAi iADC Global Competitive Landscape of KRAS G12C Inhibitors Indications Product ≥2L NSCLC 1L NSCLC ≥2L PDAC ≥3L CRC Multi-tumors monotherapy combo with JAB-3312 monotherapy combo with cetuximab basket mono Pivotal trial started in Impressive Phase III regis

  12. Slide 12: Cross Trial Comparison with Marketed KRAS G12Ci Monotherapy in ≥ 2L NSCLC

    KRAS G12Ci SHP2i KRASmultii p53a BETi AURKAi iADC Cross Trial Comparison with Marketed KRAS G12Ci Monotherapy in ≥ 2L NSCLC Efficacy Safety Product ORR mPFS ≥G3 TRAE Major GI TRAE diarrhea: 4.5% Glecirasib1 42.5% 9.6 m 23% nausea: 5.7% (Jacobio) (17/40) vomiting: 2.9% diarrhea: 31.7% Sotorasib2 28.1

  13. Slide 13: Competitive Landscape of KRAS G12Ci in ≥2L PDAC

    KRAS G12Ci SHP2i KRASmultii p53a BETi AURKAi iADC Competitive Landscape of KRAS G12Ci in ≥2L PDAC Treatment ORR (%) mPFS (m) mOS (m) ≥Gr3 TRAE Data Source Glecirasib 41.9% 5.6 10.7 25% 2024 ASCO GI (Jacobio) (14/31) Sotorasib 21% 4.0 6.9 15.8% CodeBreaK1001 (Amgen) Adagrasib 33.3% 5.4 8.0 27% KRYSTA

  14. Slide 14: Impressive Clinical Outcome of Glecirasib Monotherapy in ≥2L Multi-Tumors Basket

    KRAS G12Ci SHP2i KRASmultii p53a BETi AURKAi iADC Impressive Clinical Outcome of Glecirasib Monotherapy in ≥2L Multi-Tumors Basket Tumor Type N Confirmed ORR, n(%) DCR, n(%) Multi-tumors basket 19 11 (57.9%) 16 (84.2%) Biliary tract cancer 7 5 (71.4%) 7 (100%) Gastric cancer 3 2 (66.7%) 3 (100%) Sma

  15. Slide 15: Competitive Landscape of KRAS G12Ci in advanced 2L CRC

    KRAS G12Ci SHP2i KRASmultii p53a BETi AURKAi iADC Competitive Landscape of KRAS G12Ci in advanced 2L CRC Company Treatment ORR (%) DCR (%) mPFS Data Source Glecirasib: 800 mg QD 33.3% (11/33) 90.9% (30/33) 6.9 m Jacobio 2023 JCA-AACR Glecirasib: 800 mg QD 62.8% (27/43) 93% (40/43) Not reached Cetuxi

  16. Slide 16: SHP2 Functions in both RAS Signaling and Immune Checkpoint Regulation

    KRAS G12Ci SHP2i KRASmultii p53a BETi AURKAi iADC SHP2 Functions in both RAS Signaling and Immune Checkpoint Regulation  SHP2 Inhibition Sensitizes Diverse Oncogene-Addicted Solid Tumors to re-Treatment with Targeted Therapy Immune checkpoint in T cells RAS pathway in tumor cells RTK PD-1 BTLA Othe

  17. Slide 17: JAB-3312: the Most Potent SHP2 Inhibitor

    KRAS G12Ci SHP2i KRASmultii p53a BETi AURKAi iADC JAB-3312: the Most Potent SHP2 Inhibitor JAB-3312 TNO155 (Reported) PF-07284892 (Reported) Biochemical 1.5 11a 21 nMc IC50 (nM) p-ERK Inhibition 0.2-1.2 11a 1.7-27 nMc IC50 (nM) Cellular Proliferation 0.7-3.0 100a Not reported IC50 (nM) Dosing Regime

  18. Slide 18: Global Competitive Landscape of SHP2i

    KRAS G12Ci SHP2i SHP2i KRASmultii p53a BETi AURKAi iADC Global Competitive Landscape of SHP2i Company Treatment Indication ORR (%) DCR (%) Data source 65.5% 100% (38/58) (58/58) KRAS G12C+ 1L NSCLC 86.7% JAB-3312: 2/3 mg QD or 100% Jacobio (13/15) 2023 ESMO intermittent glecirasib (15/15) RP2D ≥2L N

  19. Slide 19: Competitive Landscape in 1L NSCLC

    KRAS G12Ci SHP2i KRASmultii p53a BETi AURKAi iADC Competitive Landscape in 1L NSCLC TRAEs caused 12Ci Treatment Indication ORR (%) DCR (%) ≥Gr3 TRAE References discontinuation Glecirasib + JAB-3312 1L NSCLC with 86.7% 100% 36.7% (N=49) 2% (N=49) 2023 ESMO (800 mg QD+2 mg [1/1]) KRAS G12C (13/15) (15

  20. Slide 20: Pivotal Trial Design for Glecirasib Combined with JAB-3312 in 1L NSCLC

    KRAS G12Ci SHP2i KRASmultii p53a BETi AURKAi iADC Pivotal Trial Design for Glecirasib Combined with JAB-3312 in 1L NSCLC Induction Therapy Maintenance Therapy Key eligibility criteria glecirasib +JAB-3312 glecirasib +JAB-3312 • Advanced or metastatic non- squamous NSCLC with KRASG12C R mutation； • P

  21. Slide 21: JAB-23E73: a First-in-Class Orally Bioavailable KRASmulti Inhibitor

    KRAS G12Ci SHP2i KRASmulti KRAS multii i p53a BETi AURKAi iADC JAB-23E73: a First-in-Class Orally Bioavailable KRASmulti Inhibitor PDAC KRAS mt total ～90% KRAS G12D ～36% KRAS G12V ～27%  23% of human cancers harbor KRAS mutations 36% KRAS  2,700,000 new cancer cases per year with KRAS G12R/S/A ～36%

  22. Slide 22: JAB-23E73 Leads to Tumor Regression in Multiple KRAS Mutant Xenografts

    KRAS G12Ci SHP2i KRASmulti KRAS multii i p53a BETi AURKAi iADC JAB-23E73 Leads to Tumor Regression in Multiple KRAS Mutant Xenografts Lung Cancer Pancreas Cancer NCI-H441 (Lung, KRAS G12V ) Xenografts Capan-2 (Pancreas, KRAS G12V) Xenografts 1400 1400 1200 1200 Tumor volume, mm3 Tumor volume, mm3 10

  23. Slide 23: Comparison between JAB-23E73 and other RAS Inhibitors

    KRAS G12Ci SHP2i KRASmultii KRASmultii p53a BETi AURKAi iADC Comparison between JAB-23E73 and other RAS Inhibitors Assay Potency JAB-23E73 BI-compound1 RMC-62362 LY40664343 GDP-KRAS (IC50) ~1 nM ~5 nM No data No data Biochemical assay GTP-KRAS (IC50) 5-150 nM ~ 5500 nM 50-500 nM 12 nM (G12V) by BiBR

  24. Slide 24: P53: the Most Commonly Mutated Gene in Cancer

    KRAS G12Ci SHP2i KRASmultii p53a p53a BETi AURKAi iADC P53: the Most Commonly Mutated Gene in Cancer  P53 is a major tumor suppressor involved in regulating multiple cellular processes, such as cell cycle arrest, DNA repair, apoptosis, senescence, etc.  P53 Y220C mutation is associated with 100,00

  25. Slide 25: JAB-30355: a Potent Oral P53 Y220C Reactivator

    KRAS G12Ci SHP2i KRASmultii p53a p53a BETi AURKAi iADC JAB-30355: a Potent Oral P53 Y220C Reactivator JAB-30355 Profile Assay JAB-30355 PMV-cmpd* Affinity KD (nM) 1.68 7.95  PMV pharma initiated a single arm Phase II pivotal trail with their p53 Y220C reactivator, Biophysics EC50 (nM) 69.70 154 PC1

  26. Slide 26: JAB-8263: a Highly Potent BET Inhibitor

    KRAS G12Ci SHP2i KRASmultii p53a BETi BETi AURKAi iADC JAB-8263: a Highly Potent BET Inhibitor MOA Preclinical study BET is a family of proteins with  JAB-8263 is a potent BET inhibitor, with an IC50 of ~0.20 nM. (IC50 of pelabresib bromodomains (BRDs). BET is from MorphoSys is ~39 nM) frequently o

  27. Slide 27: MF Case Report

    KRAS G12Ci SHP2i KRASmultii p53a BETi AURKAi iADC MF Case Report One MF patient treated with 0.125 mg JAB-8263 QD  SVR improvement: 33% at 2.5 m, 50.22% at 8.5 m  TSS improvement: MPN-SAF 34 (baseline) ~ 6 (C3D1), MPN-SAF 34 (baseline)~ 5(C10D1) 27

  28. Slide 28: JAB-8263: the Most Potent BET Inhibitor in Clinical Development

    KRAS G12Ci SHP2i KRASmultii p53a BETi BETi AURKAi iADC JAB-8263: the Most Potent BET Inhibitor in Clinical Development JAB-8263 Pelabresib1 BMS-9861582 0.3~0.4 mg QD 125 mg QD 0.5~3.75 mg QD Clinical dosage consecutive 14 d on/7 d off 5 d on/2 d off  Phase 3 study of pelabresib (CPI-0610, MorphoSys

  29. Slide 29: JAB-2485: a Highly Selective Aurora Kinase A Inhibitor

    KRAS G12Ci SHP2i KRASmultii p53a BETi AURKAi AURKAi iADC JAB-2485: a Highly Selective Aurora Kinase A Inhibitor MOA Preclinical study Aurora kinase A (AURKA) is  JAB-2485 is a highly potent AURKA inhibitor, with 1500-fold selectivity over a regulator of mitosis, and AURKB and AURKC also participate

  30. Slide 30: Immuno-oncology

    Immuno-oncology iADC: STING agonist as a Novel Payload 2022 Annual Results

  31. Slide 31: STING Agonist Reprograms TME to Overcome ICI Resistance

    KRAS G12Ci SHP2i KRASmultii p53a BETi AURKAi iADC iADC STING Agonist Reprograms TME to Overcome ICI Resistance and Convert “Cold” Tumors into “Hot” Tumors Rational 作用机制 iADCs promote immune cell infiltration into solid tumors, and boost antitumor immunity  iADCs targeted deliver STING agonists into

  32. Slide 32: JAB-BX400 (HER2-STING) is Effective in Cold Tumor and DS-8201 Resistant Tumor Models

    KRAS G12Ci SHP2i KRASmultii p53a BETi AURKAi iADC iADC JAB-BX400 (HER2-STING) is Effective in Cold Tumor and DS-8201 Resistant Tumor Models Cold tumor Model DS-8201 Resistant Tumor Model JAB-BX400 (HER2-STING iADC) and XMT-2056 BX400 (HER2-STING iADC) is effective in DS8201 (Mersana’s HER2-STING iAD

  33. Slide 33: On Target to Capture the Global Market

    On Target to Capture the Global Market 2022 Annual Results

  34. Slide 34: FY23 Financial Highlights

    FY23 Financial Highlights R&D Expenses 3-Year Cash Runway Major Cash Flow Items 446 （RMB Million) Cash flows generated from operating and financing 372 2022/12/31 1300 activities – RMB342 million -16.5%  RMB139M from share placement  RMB70M from AbbVie collaboration 2023/12/31 1200 270  RMB60M fr

  35. Slide 35: Company Strategy

    Company Strategy FIC & Global Top 3 In-house R&D Global Market Key projects on validated Focus on in-house R&D by Explore MNC partnership oncogenic signaling leveraging our IADD and iADC to capture global market pathways rank among platforms the top three in the world 35

  36. Slide 36: Thank you!

    Thank you! 2022 Annual Results

Jacobio Pharmaceuticals Group — FY2023 Earnings Presentation on 6ix